ArticleCirculation research2023
Hydrogen Sulfide Modulates Endothelial-Mesenchymal Transition in Heart Failure.
Article in Circulation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Novel Quality Metrics for Assessing the Reproducibility and Translational Relevance of Mouse Transverse Aortic Constriction Experiments: A Systematic Review.Journal of the American Heart Association · 2026Pooled it
- Molecular Mechanisms Governing Vascular Function in Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Combination of genetic eNOS deficiency and high-fat diet induces reproducible cardiometabolic HFpEF.Redox biology · 2026Article
- Human iPSC-Derived Vascularised Lung Organoids for Modelling COPD and Pulmonary Hypertension.Cell proliferation · 2026Article
- Targeting Integrin β3 in Endothelial Cells Attenuates Cardiac Fibrosis Through the Calcium-Calmodulin-Dependent Protein Kinase IIα- cAMP-Responsive Element Binding Protein 1 Signaling Axis in Pressure Overload-Induced Heart Failure.Journal of the American Heart Association · 2026Article
- The impact of inflammation, neuromodulation, and gut microbiota on developing cardiac fibrosis and hypertension.Cardiovascular research · 2026Review
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Sex-Specific Exosome Cargo Reveals Potential New Mechanisms of Salt-Sensitive Hypertension.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Design of RGD-functionalized GSH-responsive pegylated polymeric protacs for selective BRD4 degradation and EndMT-driven cardiac fibrosis inhibition.Journal of nanobiotechnology · 2026Article
- Chemogenetic Manipulation of HPrecision chemistry · 2026Article
- Parkin-ACSL4 axis in ferroptosis regulation: a narrative review on therapeutic insights from exercise in aging cardiomyocytes.npj metabolic health and disease · 2026Review
- Hydrogen sulfide improves vascular endothelial function in hypertensive states through SIRT6 anti-inflammatory signaling.Acta biochimica et biophysica Sinica · 2025Article
- Cystathionine γ lyase deletion enhances corpus cavernosum contraction via thromboxane AAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Targeting pyroptosis in myocardial inflammation and fibrosis: molecular mechanisms and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2025Review
- Hydrogen Sulfide Deficiency and Therapeutic Targeting in Cardiometabolic HFpEF: Evidence for Synergistic Benefit With GLP-1/Glucagon Agonism.JACC. Basic to translational science · 2025Article
- Hydrogen sulfide aggravates neutrophil infiltration, vascular remodeling and elastase-induced abdominal aortic aneurysm in male mice.Communications medicine · 2025Article
- Loganin ameliorates left ventricular fibrosis and dysfunction induced by pressure overload via the Sirt1/AKT/TGF-β1 signaling pathway.Journal of natural medicines · 2025Article
- Targeted codelivery of nitric oxide and hydrogen sulfide for enhanced antithrombosis efficacy.Bioactive materials · 2025Article
- Alcohol-induced gut microbial reorganization and associated overproduction of phenylacetylglutamine promotes cardiovascular disease.Nature communications · 2024Article
- Adjunctive therapy with an oral HBritish journal of pharmacology · 2024Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
backgroundHydrogen sulfide is a critical endogenous signaling molecule that exerts protective effects in the setting of heart failure. Cystathionine γ-lyase (CSE), 1 of 3 hydrogen-sulfide-producing enzyme, is predominantly localized in the vascular endothelium. The interaction between the endothelial CSE-hydrogen sulfide axis and endothelial-mesenchymal transition, an important pathological process contributing to the formation of fibrosis, has yet to be investigated.
methodsEndothelial-cell-specific CSE knockout and Endothelial cell-CSE overexpressing mice were subjected to transverse aortic constriction to induce heart failure with reduced ejection fraction. Cardiac function, vascular reactivity, and treadmill exercise capacity were measured to determine the severity of heart failure. Histological and gene expression analyses were performed to investigate changes in cardiac fibrosis and the activation of endothelial-mesenchymal transition.
resultsEndothelial-cell-specific CSE knockout mice exhibited increased endothelial-mesenchymal transition and reduced nitric oxide bioavailability in the myocardium, which was associated with increased cardiac fibrosis, impaired cardiac and vascular function, and worsened exercise performance. In contrast, genetic overexpression of CSE in endothelial cells led to increased myocardial nitric oxide, decreased endothelial-mesenchymal transition and cardiac fibrosis, preserved cardiac and endothelial function, and improved exercise capacity.
conclusionsOur data demonstrate that endothelial CSE modulates endothelial-mesenchymal transition and ameliorate the severity of pressure-overload-induced heart failure, in part, through nitric oxide-related mechanisms. These data further suggest that endothelium-derived hydrogen sulfide is a potential therapeutic for the treatment of heart failure with reduced ejection fraction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.